Mob ntshav qab zib thaum ntxov thiab lig dhau los

Kev mob lig tshwm sim hauv ob hom ntshav qab zib. Kev kuaj mob, tsib qhov loj kawg ntawm cov mob ntshav qab zib yuav txawv: macroangiopathy, nephropathy, retinopathy, neuropathy, thiab mob ko taw mob ntshav qab zib. Qhov tsis yog-tshwj xeeb ntawm cov teeb meem lig rau qee yam ntshav qab zib yog txiav txim siab los ntawm qhov tseeb tias lawv cov kab mob tseem ceeb pathogenetic txuas yog mob hyperglycemia. Hauv qhov no, thaum lub sijhawm tshwm sim ntawm CD-1, cov teeb meem tom qab hauv cov neeg mob yuav luag ib txwm tsis tshwm sim, tsim tom qab xyoo thiab xyoo lawm, nyob ntawm qhov siv tau ntawm kev kho. Tus nqi kho mob siab tshaj plaws hauv cov ntshav qab zib-1, raws li txoj cai, kis tau cov kab mob ntshav qab zib microangiopathy (nephropathy, retinopathy) thiab neuropathy (mob ntshav taw ko taw). Hauv DM-2, ntawm qhov tsis tooj, qhov teeb meem tom qab feem ntau pom muaj twb tau nyob rau lub sijhawm kev kuaj mob. Firstly, qhov no yog vim qhov tseeb tias SD-2 ua tau nws tus kheej ntev ua ntej kev kuaj mob tau tsim. Thib ob, atherosclerosis, kuaj pom los ntawm macroangiopathy, muaj ntau yam pathogenesis txuas nyob rau hauv ntau nrog ntshav qab zib. Ntawm ntshav qab zib mellitus-2, mob ntshav qab zib macroangiopathy, uas thaum lub sijhawm kuaj yog kuaj pom nyob rau feem ntau ntawm cov neeg mob. Hauv txhua kis, teeb thiab mob hnyav ntawm tus neeg cov teeb meem qeeb dhau los sib txawv ntawm lawv qhov tsis sib xws tag nrho, txawm tias lub sijhawm tseem ceeb ntawm tus kabmob, mus txog rau kev sib txuas ntawm txhua qhov kev xaiv nyob rau hauv daim ntawv hnyav.

Kev mob lig yog qhov tseem ceeb ua tuag cov neeg mob ntshav qab zib, thiab coj mus rau hauv nws tus kheej nthuav dav - qhov teeb meem kev kho mob thiab kev noj qab haus huv tseem ceeb hauv ntau lub tebchaws. Hauv qhov no lub hom phiaj tseem ceeb ntawm kev kho mob thiab kev soj ntsuam ntawm cov neeg mob ntshav qab zib yog kev tiv thaiv (thawj, theem nrab, qib 3) ntawm nws cov kev mob lig.

7.8.1. Ntshav qab zib macroangiopathy

Ntshav qab zib macroangiopathy - ib lub tswvyim kev sib xyaw ua ke uas muaj cov atherosclerotic lesions ntawm cov hlab ntsha loj hauv ntshav qab zib, qhov chaw kho mob tshwm sim los ntawm kev mob plawv hauv lub plawv (CHD), obliterating atherosclerosis ntawm cov hlab ntsha ntawm lub paj hlwb, qis qis dua, sab hauv nruab nrog thiab cov hlab ntshav siab (Cov Lus 7.16).

Tab. 7L6. Ntshav qab zib macroangiopathy

Etiology thiab pathogenesis

Hyperglycemia, hlab ntsha tawg, dyslipidemia, kev rog, insulin tsis kam, hypercoagulation, endothelial kawg, oxidative kev nyuaj siab, kab mob ntawm lub cev

Txoj kev pheej hmoo ntawm kev tsim mob plawv mob ntshav qab zib nrog ntshav qab zib hom 2 yog 6 npaug ntau dua li ntawm txoj kev tsis muaj ntshav qab zib. Arterial hypertension tau tshawb pom hauv 20% ntawm cov neeg mob uas muaj ntshav qab zib hom 1 thiab 75% ntawm cov neeg mob ntshav qab zib hom 2. Peripheral arteriosclerosis nyob rau hauv cov hlab ntsha peripheral kev loj hlob hauv 10%, thiab cov hlab hlwb hauv 8% ntawm cov neeg mob ntshav qab zib

Lub ntsiab soj ntsuam tshwm sim

Zoo ib yam li cov neeg nyob hauv cov tsis muaj ntshav qab zib. Nrog ntshav qab zib myocardial infarction hauv 30% ntawm cov neeg mob tsis hnov ​​mob

Zoo ib yam li cov neeg nyob hauv cov tsis muaj ntshav qab zib.

Lwm yam kab mob plawv, tsos mob ntsig txog hlab ntsha tawg, theem siab dyslipidemia

Antihypertensive kev kho, kev kho ntawm dyslipidemia, kev kho mob antiplatelet, tshuaj ntsuam thiab kho kab mob plawv

Kab mob plawv tuag 75% ntawm cov neeg mob ntshav qab zib hom 2 thiab 35% ntawm cov neeg mob ntshav qab zib hom 1

Etiology thiab pathogenesis

Tej zaum, qhov etiology thiab pathogenesis ntawm atherosclerosis ntawm txoj kev tsis muaj ntshav qab zib yog qhov zoo sib xws. Atherosclerotic plaques tsis txawv hauv cov qauv me me ntawm txoj kev nrog thiab tsis muaj ntshav qab zib. Txawm li cas los xij, nyob rau hauv ntshav qab zib, lwm cov kev pheej hmoo yuav tuaj yeem dhau los, lossis ntshav qab zib ua rau cov neeg mob ntshav tsis muaj qhov ua rau pom. Cov muaj ntshav qab zib yuav tsum muaj:

1. Kev mob siab. Nws yog qhov phom sij txaus rau kev txhim kho atherosclerosis. 1% nce rau HbAlc hauv cov neeg mob ntshav qab zib hom 2

Muaj qhov 15% pheej hmoo ntawm kev tsim mob myocardial infarction. Lub tshuab ntawm cov nyhuv atherogenic ntawm hyperglycemia tsis tau paub meej tag nrho; nws yuav cuam tshuam nrog glycation ntawm cov khoom kawg metabolic ntawm LDL thiab collagen ntawm phab ntsa vascular.

Arterial tawg (AH). Hauv pathogenesis, zoo qhov tseem ceeb yog txuas rau lub raum tivthaiv (mob ntshav qab zib nephropathy). Kev mob ntshav qab zib hauv ntshav qab zib-2 tsis muaj tsawg dua qhov kev pheej hmoo rau lub plawv nres thiab mob hlab ntsha tawg dua hyperglycemia.

Dyslipidemia. Hyperinsulinemia, uas yog qhov tseem ceeb ntawm insulin kuj nyob rau hauv DM-2, ua rau HDL txo qis, nce hauv triglycerides thiab txo qis hauv ntom, i.e. nce atherogenicity ntawm LDL.

Kev pham, uas cuam tshuam rau cov neeg mob feem ntau uas mob ntshav qab zib hom 2, nws yog ib qho kev pheej hmoo ntawm tus mob atherosclerosis, myocardial infarction, thiab mob stroke (saib kab lus 11.2).

Insulin kuj. Hyperinsulinemia thiab qib siab ntawm insulin-proinsulin zoo li cov lwg me me ua rau muaj kev pheej hmoo ntawm kev tsim mob atherosclerosis, uas tej zaum yuav cuam tshuam nrog endothelial kawg.

Ua txhaum ntawm cov ntshav coagulation. Nrog rau cov ntshav qab zib, qhov nce ntxiv ntawm cov qib fibrinogen, tus ua haujlwm ntawm lub platelet inhibitor thiab von Willebrand factor, tau txiav txim siab, qhov txiaj ntsig ntawm qhov uas prothrombotic lub xeev ntawm cov ntshav coagulating tsim.

Endothelial kawg, tsiag ntawv los ntawm nce kev qhia ntawm plasminogen inhibitor activator thiab cell adhesion molecules.

Oxidative kev nyuaj siab, ua rau muaj kev nce ntxiv hauv cov kev coj ua ntawm oxidized LDL thiab P2-isoprostanes.

Mob voos nyob rau hauv uas muaj kev nce ntxiv hauv kev hais tawm ntawm fibrinogen thiab C-reactive protein.

Cov teeb meem pheej hmoo tseem ceeb tshaj plaws rau kev txhim kho mob plawv mob ntshav qab zib nrog hom ntshav qab zib hom 2 yog nce LDL, qis HDL, ntshav siab, hyperglycemia, thiab haus luam yeeb. Ib qho ntawm qhov sib txawv ntawm cov txheej txheem atherosclerotic hauv ntshav qab zib yog qhov ntau dua lub idal qhov ntawm txhab occlusive, i.e. Kev sib koom tes ntawm cov hlab ntsha me feem ntau koom nrog cov txheej txheem, uas ua rau kev kho mob phais sai thiab ua rau muaj kev mob ntshav siab.

Txoj kev pheej hmoo ntawm kev tsim mob plawv mob plawv rau cov neeg muaj ntshav qab zib hom 2 yog 6 npaug ntau dua rau cov neeg tsis muaj ntshav qab zib, thaum nws tseem zoo ib yam rau cov txiv neej thiab poj niam. Arterial hypertension tau tshawb pom hauv 20% ntawm cov neeg mob uas muaj ntshav qab zib hom 1 thiab 75% ntawm cov neeg mob ntshav qab zib hom 2. Feem ntau, hauv cov neeg mob ntshav qab zib, nws tshwm sim 2 zaug ntau dua li txoj kev tsis muaj nws. Peripheral arteriosclerosis obliterans kev loj hlob hauv 10% ntawm cov neeg mob ntshav qab zib. Thromboembolism ntawm cov hlab ntsha hlwb tau nthuav dav hauv 8% ntawm cov neeg mob ntshav qab zib (2-4 zaug ntau dua li cov neeg tsis muaj ntshav qab zib).

Feem ntau, lawv tsis txawv ntawm cov kev uas tsis muaj ntshav qab zib. Hauv daim duab soj ntsuam ntawm CD-2, mob macrovascular (myocardial infarction, mob hlab ntsha tawg, mob txhab nqaij ntawm cov ceg ntawm ob txhais ceg) feem ntau tuaj rau qhov tsis nco qab, thiab nws yog thaum lawv txoj kev loj hlob uas tus neeg mob feem ntau pom tus mob hyperglycemia. Tej zaum, vim muaj tus kab mob paj hlwb tsis xis nyob, nce txog 30% ntawm myocardial infarction nyob rau hauv kev nrog ntshav qab zib ua mus tsis muaj kev raug mob ntawm lub plawv nres (tsis mob lub plawv).

Cov hauv paus ntsiab lus ntawm kev kuaj mob ntawm cov mob atherosclerosis (CHD, kev ua xiam hlwb, mob nqaij hlav hauv cov leeg ntshav) tsis txawv ntawm cov rau cov neeg tsis muaj ntshav qab zib. Kev Ntsuas ntshav siab (BP) yuav tsum tau ua nyob rau txhua zaus tuaj ntsib tus neeg mob ntshav qab zib rau tus kws kho mob, thiab kev txiav txim siab ntawm qhov ntsuas lipid spectrum ntshav (tag nrho cov cholesterol, triglycerides, LDL, HDL) rau cov ntshav qab zib yuav tsum tau nqa tawm tsawg kawg ib xyoos ib zaug.

Lwm yam kab mob plawv, tsos mob ntsig txog hlab ntsha tawg, theem siab dyslipidemia.

Tswj ntshav siab. Qeb kom tsim nyog ntawm cov ntshav ntshav systolic nyob rau hauv cov ntshav qab zib yog qis dua 130 MMHg, thiab cov tshuaj diastolic yog 80 MMHg (Cov Lus 7.3). Cov neeg mob feem ntau xav tau ntau yam tshuaj tiv thaiv kabmob txhawm rau kom ua tiav lub hom phiaj no. Cov tshuaj rau xaiv los tiv thaiv kev kho mob ntshav qab zib rau cov ntshav qab zib yog ACE inhibitors thiab angiotensin receptor blockers, uas tau ntxiv nrog thiazide diuretics, yog tias tsim nyog. Cov tshuaj ntawm kev xaiv rau cov neeg mob ntshav qab zib tom qab myocardial infarction yog P-blockers.

Kev kho ntawm dyslipidemia. Cov theem ntsuas ntawm lipid spectrum ntsuas tau nthuav tawm hauv lub rooj. 7.3. Cov tshuaj uas xaiv rau kev kho hypolipidemic yog inhibitors ntawm 3-hydroxy-3-methylglutaryl-CoA reductase (statins).

Antiplatelet Kev kho. Aspirin txoj kev kho (75-100 mg / hnub) yog qhia rau cov neeg mob ntshav qab zib laus dua 40 xyoo nrog kev pheej hmoo ntawm kev mob plawv (keeb kwm tsev neeg, mob ntshav siab, haus luam yeeb, dyslipidemia, microalbuminuria), zoo li txhua tus neeg mob uas muaj kev soj ntsuam kab mob atherosclerosis zoo li kev tiv thaiv theem nrab.

Kev kuaj mob thiab kev kho tus kab mob plawv. Kev ntsuam xyuas kev nyuaj siab kom tsis suav cov kab mob rau cov ntshav plawv tau qhia rau cov neeg mob uas muaj cov tsos mob ntawm lub plawv, nrog rau kev kuaj pom cov kab mob nrog rau ECG.

Los ntawm cov kab mob plawv, 75% ntawm cov neeg mob ntshav qab zib hom 2 thiab 35% ntawm cov neeg mob ntshav qab zib hom 1 tuag, kwv yees li 50% ntawm cov neeg mob ntshav qab zib hom 2 tuag los ntawm kev mob ntshav siab ntawm lub plawv, thiab 15% ntawm cov neeg mob hlwb txha caj qaum. Kev tuag ntawm myocardial infarction hauv cov neeg muaj ntshav qab zib ntau dua 50%.

7.8.2. Ntshav Qab Zib Retinopathy

Ntshav Qab Zib Retinopathy (DR) - retinal vascular microangiopathy, cim los ntawm kev txhim kho ntawm microaneurysms, hemorrhages, exudative hloov thiab loj hlob ntawm cov nkoj tsim tshiab, ua rau muaj feem lossis tsis pom kev (cov lus 7.17).

Lub ntsiab tseem ceeb hauv kev txhim kho ntawm DR yog mob hyperglycemia. Lwm yam (arterial hypertension, dyslipidemia, haus luam yeeb, cev xeeb tub, thiab lwm yam) tsis tshua tseem ceeb.

Cov kev sib txuas tseem ceeb hauv cov pathogenesis ntawm DR yog:

retinal vascular microangiopathy, ua rau txoj kev nqaim ntawm lub lumen ntawm cov hlab ntsha nrog kev txhim kho hypoperfusion, vascular degeneration nrog kev tsim ntawm microaneurysms, hypoxia hnyav zuj zus, txhawb kev tawm tsam vascular thiab ua rau cov roj ntsha tsis zoo thiab ua kom cov calcium ntsev hauv cov retina,

microinfarction nrog exudation, ua rau qhov tsim ntawm mos "paj rwb me ntsis",

Tab. 7.17. Ntshav Qab Zib Retinopathy

Etiology thiab pathogenesis

Chronic hyperglycemia, mob txeeb zig ntawm cov hlab ntsha microangiopathy, mob hlwb retinal ischemia thiab neovascularization, tsim cov hlab ntsha o, vitreoretinal traction, retinal detachment thiab ischemic retinal degeneration

Feem ntau ua rau pom kev dig muag ntawm cov pej xeem ua hauj lwm. Tom qab 5 xyoo, CD-1 raug tshawb pom hauv 8% ntawm cov neeg mob, thiab tom qab 30 xyoo hauv 98% ntawm cov neeg mob. Thaum lub sijhawm kuaj mob, CD-2 raug kuaj pom hauv 20-40% ntawm cov neeg mob, thiab tom qab 15 xyoo - hauv 85%. Nrog CD-1, kev nthuav dav retinopathy kuj muaj ntau, thiab nrog CD-2, maculopathy (75% ntawm cov neeg mob maculopathy)

Lub ntsiab soj ntsuam tshwm sim

Tsis-proliferative, preproliferative, proliferative retinopathy

Kev kuaj mob Ophthalmological yog qhia rau cov neeg mob ntshav qab zib hom 1 nyob rau hauv 3-5 xyoos tom qab pom tus mob, thiab rau cov neeg mob ntshav qab zib hom 2 tam sim ntawd tom qab nws kuaj pom. Nyob rau hauv lub neej yav tom ntej, cov kev tshawb fawb zoo li no yuav tsum tau rov ua txhua xyoo

Lwm cov kab mob qhov muag hauv cov neeg mob ntshav qab zib

DM them nyiaj, laser photocoagulation

Qhov muag tsis pom kev tau teev tseg hauv 2% ntawm cov neeg mob ntshav qab zib. Ntau zaus cov neeg mob dig muag tshiab uas cuam tshuam nrog DR yog 3.3 tus neeg nyob rau 100,000 tus neeg tauj ib xyoos. Nrog DM-1, qhov txo qis hauv HbAlc txog 7.0% ua rau txo 75 feem pua ​​ntawm kev pheej hmoo ntawm kev tsim D thiab 60% txo qhov txaus ntshai ntawm DR. Nrog DM-2, qhov txo qis 1% hauv HbAlc ua rau txo qis 20% txo qhov phom sij ntawm kev txhim kho DR

lipid deposition nrog kev tsim ntawm ntom exudates, ua kom loj hlob ntawm cov hlab ntsha hauv cov retina nrog kev tsim ntawm shunts thiab aneurysms, ua rau cov hlab ntsha kdilatation thiab kev tsim txom ntawm retinal hypoperfusion,

tus raug tub sab nyiag nrog kev nruam ntej ntawm ischemia, uas yog qhov ua kom muaj kev tsim cov infiltrates thiab nti,

retinal detachment raws li ib qho tshwm sim ntawm nws cov ischemic kev sib cais thiab kev tsim ntawm vitreoretinal traction,

mob ntshav tawm hauv lub cev los ntawm cov ntshav tawm ntawm lub plawv, muaj kev tawm tsam vias loj thiab cov leeg pob txha caj qaum, ua kom muaj hlab ntaws ntawm cov hlab ntsha ntawm cov ntshav (mob ntshav qab zib rubeosis), ua rau muaj kev txhim kho ntawm cov kab mob qog ntshav siab, maculopathy nrog kev mob txhav ntxiv.

DR yog qhov ua rau ntau qhov muag tsis pom kev ntawm cov neeg muaj peev xwm ntawm cov teb chaws vam meej, thiab qhov kev pheej hmoo ntawm kev txhim kho qhov muag tsis pom kev hauv cov neeg mob ntshav qab zib yog 10-20 npaug ntau dua li cov pej xeem. Thaum lub sijhawm kuaj mob CD-1, DR tsis pom nyob rau yuav luag txhua ntawm cov neeg mob, tom qab 5 xyoo, tus kab mob tau pom hauv 8% ntawm cov neeg mob, thiab nrog peb caug xyoo ntawm cov ntshav qab zib - hauv 98% ntawm cov neeg mob. Thaum lub sijhawm kuaj mob CD-2, DR raug kuaj pom ntawm 20-40% ntawm cov neeg mob, thiab ntawm cov neeg mob uas muaj kaum tsib xyoo ntawm CD-2, nyob hauv 85%. Nrog CD-1, kev nthuav dav retinopathy kuj muaj ntau, thiab nrog CD-2, mob maculopathy (75% ntawm cov neeg mob maculopathy).

Raws li kev faib tawm feem ntau lees txais, 3 theem ntawm DR tau txawv (Cov Lus 7.18).

Kev soj ntsuam ophthalmological tiav, suav nrog ophthalmoscopy ncaj qha nrog thaij duab retina, yog qhia rau cov neeg mob ntshav qab zib hom 3 years5 xyoos tom qab pom tus mob, thiab rau cov neeg mob ntshav qab zib hom 2, tam sim ntawd tom qab kuaj pom. Nyob rau hauv lub neej yav tom ntej, cov kev tshawb fawb zoo li no yuav tsum tau rov ua txhua xyoo.

Tab. 7.18. Ntawm Cov Mob Ntshav Qab Zib Retinopathy

Microaneurysms, hemorrhages, edema, exudative foci hauv retina. Hemorrhages muaj daim ntawv ntawm cov dot me me, duav, lossis tsaus me ntsis ntawm cov duab sib npaug, hauv ib cheeb tsam hauv nruab nrab ntawm cov nyiaj pob los yog raws cov tsiaj ntawv loj hauv qhov tob ntawm qhov retina. Cov ntaub ntawv tawv tawv thiab tawv sab hauv feem ntau yog nyob hauv nruab nrab ntawm qhov fundus thiab muaj daj lossis dawb. Ib qho tseem ceeb ntawm cov qib no yog retinal edema, uas yog thaj chaw hauv thaj av macular lossis raws cov nkoj loj (Daim duab 7.11 a)

Venous anomalies: ntse, tortuosity, looping, doubling thiab tshaj tawm nyob rau hauv lub caliber ntawm cov hlab ntshav. Qhov loj ntawm cov khoom thiab "paj rwb" exudates. Kev phais mob microvascular tsis nco qab ntshav, ntau lub qog ua mob loj (Daim Duab 7.11 b)

Neovascularization ntawm optic disc thiab lwm qhov chaw ntawm retina, vitreous hemorrhage, qhov tsim ntawm cov nqaij mos hauv thaj chaw ntawm preretinal hemorrhages. Cov nkoj tsim tshiab txho nyias heev thiab tsis yooj yim, qhov tshwm sim ntawm qhov uas pheej rov hem cov ntshav feem ntau tshwm sim. Vitreoretinal traction ua rau kom cov leeg rov qab los. Cov nkoj tshiab uas tsim los ntawm cov xim (iris (rubeosis)) feem ntau yog qhov ua rau muaj kev txhim kho ntawm cov kab mob glaucoma theem nrab (Daim duab 7.11 c)

Lwm cov kab mob qhov muag hauv cov neeg mob ntshav qab zib.

Lub hauv paus ntsiab lus ntawm kev kho mob ntshav qab zib, nrog rau lwm cov kev mob lig, yog qhov kev them nyiaj zoo tshaj plaws rau ntshav qab zib. Qhov kev kho mob zoo tshaj plaws rau cov ntshav qab zib muaj ntshav qab zib thiab kev tiv thaiv ntawm kev dig muag yog laser photocoagulation. Lub Hom Phiaj

- tawv exudative txhab

1 - kev tsim ntawm mos exudative foci, 2 - tus tortuosity ntawm cov hlab ntshav, 3 - mos exudative foci, 4 - retinal hemorrhages

1 - papillary neoplasms hauv thaj av ntawm lub optic disc, 2 - retinal hemorrhages, 3 - kev loj hlob ntawm neoplasms, 4 - leeg ntawm tsis ncaj caliber

Daim duab.7.11. Retinopathy uas mob ntshav qab zib:

a) non-proliferative, b) preproliferative, c) proliferative

Laser photocoagulation yog qhov xaus ntawm kev ua haujlwm ntawm cov nkoj tsim tshiab, uas ua rau muaj kev hem thawj loj rau kev txhim kho ntawm cov kev mob hnyav xws li hemophthalmus, traction retinal detachment, iris rubeosis thiab glaucoma ntxiv.

Cov dig muag tau tso npe rau 2% ntawm cov neeg mob ntshav qab zib (3-4% ntawm cov neeg mob ntshav qab zib hom 1 thiab 1.5-2% ntawm cov neeg mob ntshav qab zib hom 2). Qhov kwv yees muaj tshwm sim ntawm cov neeg mob dig muag tshiab uas cuam tshuam nrog DR yog 3.3 muaj rau 100,000 tus pej xeem nyob hauv ib xyoos. Nrog CD-1, qhov txo qis hauv HbAlc rau 7.0% ua rau qhov txo qis ntawm kev pheej hmoo ntawm kev tsim DR ntawm 75% thiab qhov txo qis ntawm kev pheej hmoo ntawm DR ntawm 60%. Nrog DM-2, qhov txo qis 1% hauv HbAlc coj mus rau 20% txo rau qhov kev pheej hmoo ntawm kev tsim DR.

7.8.3.Ntshav Qab Zib Nepropathy

Ntshav Qab Zib Nepropathy (DNF) yog txhais tias yog albuminuria (ntau dua 300 mg ntawm albumin ib hnub lossis proteinuria ntau dua 0.5 g ntawm cov protein ib hnub) thiab / lossis txo qis ntawm kev ua haujlwm ntawm lub raum hauv cov neeg mob ntshav qab zib tsis ua mob txeeb zig, mob plawv lossis lwm yam kab mob hauv lub raum. Microalbuminuria yog txhais tau tias kev tso tawm ntawm albumin 30-300 mg / hnub lossis 20-200 μg / min.

Etiology thiab pathogenesis

Cov kev pheej hmoo txaus ntshai rau DNF yog lub sijhawm mob ntshav qab zib, mob ntshav qab zib, mob ntshav qab zib, mob ntshav qis, ntshav tsis ua hauj lwm, thiab mob raum hauv niam txiv. Thaum DNF feem ntau cuam tshuam glomerular cuab yeej ob lub raum.

Ib tug tau mechanism los ntawm uas hyperglycemia pab txhawb kev txhim kho ntawm glomerular kev puas tsuaj, yog kev tsub zuj zuj ntawm sorbitol vim tias kev ua kom lub zog ntawm cov polyol ntawm cov metabolism hauv qabzib, nrog rau cov lej ntawm cov khoom lag luam kawg ntawm glycation.

Hemodynamic ntshawv siab, namely intracranial leeg ntshav siab (nce ntshav siab sab hauv glomeruli ntawm lub raum) yog qhov tseem ceeb ntawm cov kab mob pathogenesis

Qhov laj thawj ntawm kev mob ntshav siab intracubular yog kev ua txhaum ntawm lub suab ntawm cov hlab ntsha: nthuav ntawm cov kabmob thiab nqaim ntawm efferent.

Qhov no, nyeg, tshwm sim nyob rau hauv tus ntawm ib tug xov tooj ntawm humoral yam, xws li angiotensin-2 thiab endothelium, raws li zoo raws li vim ib tug ua txhaum ntawm lub electrolyte thaj chaw ntawm glomerular qab daus daim nyias nyias. Ib qho ntxiv, cov kev mob ntshav siab, uas tau txiav txim siab hauv feem ntau cov neeg mob DNF, pab txhawb kev mob ntshav siab ntawm leeg. Raws li ib qho txiaj ntsig ntawm kev mob ntshav siab hauv plab-puas tsuaj, kev puas tsuaj rau hauv qab daus daim nyias nyias thiab cov qhov hws ntxeem tau tshwm sim, dhau ntawm txeem kab (microalbuminuria), thiab tom qab ntawv tus nqi tseem ceeb ntawm albumin (proteinuria). Lub thickening ntawm hauv qab daus daim nyias nyias ua rau muaj kev hloov pauv hauv lawv cov khoom siv hluav taws xob, uas nyob rau hauv nws tus kheej coj mus rau lub ingress ntawm ntau albumin mus rau hauv ultrafiltrate txawm tias qhov tsis muaj qhov hloov pauv ntawm qhov loj ntawm lub qhov hws.

Tab. 7. Peb muaj 7.19. Ntshav Qab Zib Nepropathy

Etiology thiab pathogenesis

Ntev hyperglycemia, mob intracubic thiab mob ntsig txog cov hlab ntsha o cov caj ces, caj ces hlav tawm

Microalbuminuria tau txiav txim siab hauv 6-60% ntawm cov neeg mob ntshav qab zib hom 1 tom qab 5-15 xyoo tom qab pom. Nrog CD-2, DNF kev tsim kho hauv 25% ntawm cov neeg European thiab 50% ntawm cov neeg Asian. Tag nrho cov kabmob ntawm DNF hauv CD-2 yog 4-30%

Lub ntsiab soj ntsuam tshwm sim

Hauv cov theem thaum ntxov tsis tuaj kawm ntawv. Arterial hypertension, mob nephrotic, mob raum tsis ua haujlwm

Microalbuminuria (albumin excretion 30-300 mg / hnub lossis 20-200 μg / min), proteinuria, nce thiab tom qab ntawd txo tus nqi glomerular pom, cov cim ntawm nephrotic syndrome thiab mob raum tsis ua haujlwm.

Lwm lub raum mob thiab cov ua mob raum tsis ua hauj lwm

Txo cov ntshav qab zib thiab mob ntshav siab, ACE inhibitors lossis angiotensin receptor blockers, pib los ntawm theem ntawm microalbuminuria, muaj protein tsawg thiab noj ntsev tsawg. Nrog rau kev tsim kho mob raum tsis ua haujlwm - hemodialysis, peritoneal lim ntshav, hloov raum

Hauv 50% ntawm cov neeg mob uas muaj mob ntshav qab zib hom 1 thiab 10% ntawm hom 2 mob ntshav qab zib nyob rau hauv uas tshawb pom proteinuria, CRF muaj kev txhim kho hauv 10 xyoo tom ntej. 15% ntawm tag nrho cov neeg tuag nyob hauv cov neeg mob uas muaj ntshav qab zib hom 1 qis dua 50 xyoo yog txuam nrog kev mob raum tsis ua haujlwm vim DNF

3.Kev tshuaj ntsuam genetic predisposition.Cov neeg mob txheeb ze nrog DNF nrog kev ua haujlwm siab ntau hauv cov hlab ntsha tshwm sim. Muaj pov thawj ntawm kev sib txheeb ntawm DNF thiab ACE gene polymorphism. Kev kuaj ntshav me me ntawm DNF qhia tawm lub ntsej muag tuab ntawm lub ntsej muag ntawm cov glomeruli, nthuav dav ntawm mesangium, nrog rau kev hloov fibrous hauv kev nqa thiab nqa cov hlab ntsha. Ntawm theem kawg, uas yog kho mob zoo sib xws nrog mob ntev lub raum tsis ua hauj lwm (CRF), focal (Kimmelstyle-Wilson) yog txiav txim siab, thiab tom qab ntawd diffuse glomerulosclerosis.

Microalbuminuria tau txiav txim siab hauv 6-60% ntawm cov neeg mob ntshav qab zib hom 1 tom qab 5-15 xyoo tom qab pom. DNF tau txiav txim siab hauv 35% ntawm cov neeg muaj ntshav qab zib hom 1, ntau zaus hauv cov txiv neej thiab cov neeg uas tau tsim muaj ntshav qab zib hom 1 qis dua 15 xyoos. Nrog CD-2, DNF kev tsim kho hauv 25% ntawm cov neeg European thiab 50% ntawm cov neeg Asian. Tag nrho kev nthuav dav ntawm DNF hauv CD-2 yog 4-30%.

Kev sim ua mob thaum ntxov uas yog ncaj qha cuam tshuam nrog DNF yog mob ntshav siab. Lwm qhov kev qhia ua kom pom tseeb yog qhov tuaj qeeb. Cov no suav nrog nephrotic syndrome thiab mob raum tsis ua haujlwm.

Kev soj ntsuam rau DNF rau cov neeg muaj ntshav qab zib yuav raug kuaj txhua xyoo microalbuminuria nrog DM-1 5 xyoos tom qab tshaj tawm cov kab mob, thiab nrog DM-2 - tam sim ntawd tom qab nws kuaj pom. Ntxiv rau, koj xav tau tsawg kawg qhov kev txiav txim siab txhua xyoo ntawm cov qib creatinine los laij glomerular tus nqi pom (SCF). SCF yuav yog suav siv cov qauv sib txawv, piv txwv, raws li tus qauv Cockcroft-Gault:

tab sis x (140 - hnub nyoog (xyoo)) x lub cev hnyav (kg)

ntshav creatinine (μmol / L)

Rau cov txiv neej: a = 1.23 (cov cai ntawm GFR 100 - 150 ml / min) Rau cov poj niam: a = 1.05 (cov cai ntawm GFR 85 - 130 ml / min)

Ntawm cov theem pib ntawm DNF, kev nce GFR tuaj yeem raug tshawb pom, uas maj mam poob qis nrog kev txhim kho kev mob raum tsis ua haujlwm. Microalbuminuria pib kuaj pom 5-15 xyoo tom qab pib mob ntshav qab zib-1, nrog ntshav qab zib-2 hauv 8-10% ntawm tus neeg mob, nws raug kuaj tam sim tom qab kuaj pom, tej zaum vim yog ntev asymptomatic ntawm tus kab mob ua ntej kuaj mob. Lub siab tshaj plaws hauv kev txhim kho overt proteinuria lossis albuminuria hauv ntshav qab zib hom 1 tshwm sim ntawm 15 txog 20 xyoo tom qab nws pib. Proteinuria qhia tau rov tsis tau DNF, uas sai dua lossis ntev dua yuav ua rau lub raum tsis ua haujlwm. Uremia nthuav dav thaj tsam li ntawm 7-10 xyoo tom qab qhov tsos pom ntawm overt proteinuria. Nws yuav tsum raug sau tseg tias GFR tsis cuam tshuam nrog cov proteinuria.

Lwm qhov ua rau cov proteinuria thiab lub raum tsis ua haujlwm rau cov neeg muaj ntshav qab zib. Feem ntau, DNF koom ua ke nrog kev mob ntshav siab, mob ntshav qab zib retinopathy lossis mob neuropathy, nyob rau hauv qhov tsis muaj qhov kev ntsuas txawv yuav tsum tau ceev faj tshwj xeeb. Hauv 10% ntawm cov neeg mob ntshav qab zib hom 1 thiab 30% ntawm cov neeg mob ntshav qab zib hom 2, proteinuria tsis cuam tshuam nrog DNF.

Conditions Cov teeb meem tseem ceeb ntawm cov thawj thiab theem nrab kev tiv thaiv

DNF yog them rau cov ntshav qab zib thiab tswj cov ntshav cov ntshav sib luag. Ib qho ntxiv, thawj prophylaxis ntawm DNF cuam tshuam txog kev txo cov protein kom tsawg - tsawg dua 35% ntawm kev noj zaub mov hauv lub cev txhua hnub.

♦ Hauv theem microalbuminuria thiab tshuaj proteinuria cov neeg mob yog kws kho mob ACE inhibitors lossis cov tshuaj tiv thaiv angiotensin receptor blockers. Nrog concomitant arterial hypertension, lawv raug xaj nyob rau hauv cov tshuaj tiv thaiv kabmob, yog tias tsim nyog nrog rau lwm cov tshuaj tiv thaiv kabmob. Nrog rau cov ntshav siab ib txwm, cov tshuaj no tau sau tseg hauv cov koob tshuaj uas tsis ua rau kev loj hlob ntawm hypotension. Ob qho ACE inhibitors (rau ntshav qab zib hom 1 thiab ntshav qab zib hom 2) thiab angiotensin receptor blockers (hom 2) pab tiv thaiv microalbuminuria los ntawm hloov mus rau proteinuria. Qee qhov xwm txheej, tawm tsam keeb kwm ntawm cov kev qhia tau hais tias, ua ke nrog them nyiaj mob ntshav qab zib los ntawm lwm qhov ntsuas, microalbuminuria yog tshem tawm. Tsis tas li ntawd, pib nrog theem ntawm microalbuminuria, nws yog ib qho tsim nyog yuav tsum tau txo qis protein tsawg dua 10% ntawm cov calories kom txhua hnub (lossis tsawg dua 0.8 grams toj ib kg ntawm lub cev hnyav) thiab ntsev tsawg dua 3 grams tauj ib hnub.

♦ Nyob rau theem CRF, Kev kho cov tshuaj kho hypoglycemic feem ntau yuav tsum tau kho. Feem ntau cov neeg mob ntshav qab zib mellitus-2 yuav tsum tau pauv mus rau kev kho mob insulin, txij li kev nkag ntawm TSP coj qhov kev pheej hmoo ntawm kev tsim muaj ntshav qab zib tsawg. Feem ntau cov neeg mob ntshav qab zib hom 1 muaj qhov xav tau insulin tsawg dua, txij li lub raum yog ib qho chaw tseem ceeb ntawm nws cov metabolism. Nrog rau qhov kev nce ntxiv hauv cov ntshav creatinine mus rau 500 μmol / L lossis ntau dua, nws yog qhov tsim nyog los nug cov lus nug ntawm kev npaj tus neeg mob rau kev ua tub rog ntxiv (hemodialysis, peritoneal dialysis) lossis phais (phais raum) kev kho mob. Hloov raum yog qhia nyob rau qib creatinine nce mus txog 600-700 μmol / L thiab qhov txo qis ntawm lub qog glomerular tsawg dua 25 ml / min, hemodialysis - 1000–1200 μmol / L thiab tsawg dua 10 ml / min, feem.

Hauv 50% ntawm cov neeg mob uas muaj mob ntshav qab zib hom 1 thiab 10% ntawm cov ntshav qab zib hom 2, uas tau tshawb pom, tus kab mob ntsws raum tsis zoo tshwm sim nyob rau 10 xyoo tom ntej. 15% ntawm tag nrho cov neeg tuag nyob hauv cov neeg mob uas muaj ntshav qab zib hom 1 qis dua 50 xyoo yog txuam nrog kev mob raum tsis ua haujlwm vim DNF.

7.8.4. Mob neuropathy mob ntshav qab zib

Mob neuropathy mob ntshav qab zib (NU) yog kev sib txuas ntawm cov sib txuam ntawm kev puas tsuaj rau cov leeg hlwb, uas tuaj yeem ua raws li cov neeg koom nrog cov txheej txheem tseem ceeb ntawm cov txheej txheem ntawm nws ntau lub chaw haujlwm (sensorimotor, autonomous), raws li qhov kis tau zoo thiab mob siab rau qhov txhab (Cov Lus 7.20).

Cov mob ntshav qab zib lig: kev tiv thaiv thiab kho mob

Mob ntshav qab zib mellitus yog ib qho txaus ntshai heev uas ua rau cov txheej txheem hauv metabolic, nrog rau cov metabolism hauv kev ua kom yuag, cuam tshuam. Tus kab mob no muaj tus mob mus ntev, thiab nws tuaj yeem kho tsis tau, tab sis nws tuaj yeem raug kho tau.

Txhawm rau kom tsis txhob tsim cov ntshav qab zib tsis txaus, nws yog ib qho tsim nyog yuav tsum tau mus cuag tus kws kho qhov muag endocrinologist thiab kws kho mob kom tsis tu ncua. Nws yog ib qho tseem ceeb uas saib xyuas qib ntawm cov piam thaj, uas yuav tsum yog li 4 txog 6.6 mmol / l.

Txhua tus neeg mob ntshav qab zib yuav tsum paub tias qhov tshwm sim ntawm tus mob hyperglycemia feem ntau ua rau muaj kev tsis taus thiab txawm tias muaj neeg tuag, tsis hais hom mob twg. Tab sis cov teeb meem ntshav qab zib yuav tuaj yeem tsim muaj li cas thiab vim li cas thiaj pom tshwm sim?

Kev mob ntshav qab zib: kev loj hlob ntawm cov tshuab

Hauv cov neeg noj qab haus huv, cov piam thaj yuav tsum nkag mus rau cov rog thiab cov leeg nqaij, muab lub zog rau lawv, tab sis cov ntshav qab zib nws tseem nyob hauv cov ntshav. Nrog cov piam thaj uas tsis tu ncua, uas yog cov tshuaj hyperosmolar, cov hlab ntsha thiab cov ntshav ntawm cov ntshav ua rau lub cev puas lawm.

Tab sis cov no twb yog mob lig ntshav qab zib. Nrog rau cov ntshav tsis txaus insulin, mob hnyav tshwm sim uas yuav tsum tau kho tam sim ntawd, vim tias lawv tuaj yeem ua rau tuag taus.

Hauv hom 1 Ntshav Qab Zib, lub cev tau ua tsis txaus ntawm cov tshuaj insulin. Yog tias qhov tshuaj hormones tsis txaus los ntawm kev kho mob insulin, tom qab ntawd qhov tshwm sim ntawm ntshav qab zib yuav pib sai sai, uas yuav txo qis txoj sia ntawm ib tug neeg.

Hauv hom ntshav qab zib hom 2, tus txiav tsim tawm insulin, tab sis cov keeb ntawm lub cev rau ib qho laj thawj lossis lwm tus tsis pom txog. Hauv qhov no, cov tshuaj txo cov ntshav qab zib tau raug sau tseg, thiab cov tshuaj uas ua rau muaj zog tiv thaiv cov tshuaj insulin, uas yuav ua rau cov metabolism hauv lub cev ua rau lub sijhawm ncua ntawm cov tshuaj.

Feem ntau, cov teeb meem loj ntawm hom 2 ntshav qab zib mellitus tsis tshwm sim los yog nws tshwm sim yooj yim dua. Tab sis feem ntau, ib tus neeg tsuas pom txog qhov muaj ntshav qab zib thaum tus kab mob mus zuj zus, thiab qhov tshwm sim tuaj yeem hloov kho tsis tau.

Yog li, mob ntshav qab zib tau muab faib ua ob pawg:

Mob hnyav

Qhov tshwm sim thaum ntxov ntawm ntshav qab zib suav nrog cov xwm txheej uas tshwm sim tawm tsam keeb kwm yav dhau los ntawm qhov kev txo qis (hypoglycemia) lossis kev lom zem (hyperglycemia) nyob rau hauv cov concentration ntawm cov piam thaj hauv cov ntshav. Lub xeev hypoglycemic txaus ntshai yog vim hais tias thaum nws tsis tuaj yeem nres, lub hlwb nqaij pib tuag.

Cov laj thawj rau nws qhov tshwm sim muaj ntau haiv neeg: kev siv tshuaj ntau dhau ntawm insulin lossis hypoglycemic, ntau dhau ntawm lub cev thiab kev ntxhov siab, hla zaub mov noj, thiab lwm yam. Tsis tas li, kev txo qis hauv qab zib feem ntau tshwm sim thaum cev xeeb tub thiab mob raum.

Cov tsos mob ntawm lub qog ntshav qab zib yog qhov mob tsis muaj zog, tshee hnyo ntawm tes, tawv nqaij daj ntseg, kiv taub hau, loog ntawm txhais tes thiab kev tshaib plab. Yog tias nyob rau theem no ib tug neeg tsis noj zaub mov sai (haus dej qab zib, khoom qab zib), tom qab ntawd nws yuav txhim kho theem tom ntej, uas yog cov tsos mob hauv qab no:

  • dev paus
  • kev koom ua ke tsis zoo
  • nkees
  • ob lub zeem muag
  • tsim txom hnyav
  • palpitations
  • flickering "goosebumps" ua ntej lub qhov muag,
  • cov mem tes ceev.

Qhov theem ob tsis kav ntev, tab sis nws muaj peev xwm pab tus neeg mob hauv qhov no yog tias koj muab kua qab zib me rau nws. Txawm li cas los xij, cov zaub mov tawv hauv qhov no yog contraindicated, vim tus neeg mob yuav muaj hlab cua txhaws.

Qhov qhia qog ntshav qog ua kom ntshav qab zib nce ntxiv tawm hws, nti, daj ntseg ntawm daim tawv nqaij, thiab tsis nco qab. Hauv cov xwm txheej no, nws yog qhov yuav tsum tau hu rau lub tsheb thauj neeg mob, thaum tuaj txog uas tus kws kho mob yuav txhaj tshuaj pleev xim rau hauv tus neeg mob txoj hlab ntshav.

Thaum tsis muaj kev kho mob sijhawm, tus neeg yuav hloov pauv siab. Thiab nyob rau hauv cov ntaub ntawv ntawm kev loj hlob ntawm coma, nws yuav txawm tuag, vim hais tias lub zog yuav tshaib plab yuav ua rau o ntawm lub hlwb hlwb thiab tom qab hemorrhage nyob rau hauv lawv.

Cov teeb meem ntshav qab zib thaum ntxov nram no yog hyperglycemic tej yam kev mob, uas suav nrog peb yam ntawm com:

  1. ketoacidotic,
  2. lacticidal,
  3. hyperosmolar.

Cov teebmeem ntshav qab zib no tshwm sim ntawm kev nce ntshav qab zib. Lawv txoj kev kho yog nqa tawm hauv tsev kho mob, hauv kev saib xyuas hnyav lossis hauv chav kho mob hnyav.

Ketoacidosis hauv ntshav qab zib hom 1 feem ntau tshwm sim txaus. Cov laj thawj rau nws tshwm sim muaj ntau yam - hla kev siv tshuaj, lossis lawv txoj kev noj tshuaj tsis raug, muaj cov mob tshwm sim hauv lub cev, mob plawv nres, mob stroke, exacerbation ntawm tus kab mob ntev, kev ua xua, thiab lwm yam.

Ketoacidotic coma kev loj hlob raws li cov qauv tshwj xeeb. Vim tias tsis muaj cov tshuaj insulin sai, cov piam thaj tsis nkag mus rau hauv lub hlwb thiab sib sau ua ke rau hauv cov ntshav. Raws li qhov tshwm sim, "kev tshaib plab" lub zog. Hauv kev teb rau nws, lub cev pib tso tawm cov kev kub ntxhov hauv cov tshuaj hormones xws li glucagon, cortisol thiab adrenaline, uas ntxiv nce hyperglycemia.

Hauv qhov no, cov ntshav nce ntxiv, vim tias cov piam thaj yog cov tshuaj osmotic uas nyiam dej. Hauv qhov no, ob lub raum pib ua haujlwm sib zog, thaum lub sijhawm xaim hluav taws xob, uas tso nrog dej, pib ntws mus rau hauv cov zis nrog qab qab zib.

Raws li qhov ua tiav, lub cev ua kom lub cev tsis muaj dej txaus, thiab lub hlwb thiab lub raum txom nyem los ntawm cov ntshav tsis zoo.

Nrog cov pa oxygen tshaib plab, lactic acid yog tsim, vim tias tus pH ua kua qaub. Vim yog qhov tseeb tias cov piam thaj tsis hloov mus ua lub zog, lub cev pib siv lub peev xwm khaws cov rog, vim qhov ntawd ketones tshwm sim hauv cov ntshav, uas ua rau cov ntshav pH ntau cov kua qaub. Qhov no tsis zoo cuam tshuam rau kev ua haujlwm ntawm lub hlwb, lub plawv, lub plab zom mov thiab lub plab ua pa.

  • Ketosis - daim tawv nqaij qhuav thiab cov leeg ua kua, nqhis dej, tsaug zog, tsis muaj zog, mob taub hau, qab los noj mov tsis zoo, tso zis ntxiv.
  • Ketoacidosis - tsis hnov ​​tsw ntawm acetone los ntawm lub qhov ncauj, tsaug zog, ntshav siab, ntuav, lub plawv dhia.
  • Precoma - ntuav, hloov pauv pa, ntsej mua nce ntshav ntawm lub puab tsaig, mob tshwm sim thaum lub sij hawm palpation ntawm lub plab.
  • Coma - ua pa nrov nrov, pallor ntawm daim tawv nqaij, daig tawv nqaij, tsis nco qab.

Hyperosmolar coma feem ntau tshwm sim hauv cov neeg laus uas muaj kev tiv thaiv kev ywj pheej ntawm tus kab mob. Qhov tshwm sim ntawm ntshav qab zib no tshwm sim tawm tsam keeb kwm ntawm lub cev qhuav dej, thaum ntxiv nrog rau cov ntshav qab zib ntau, cov concentration ntawm sodium nyob rau hauv cov ntshav nce ntxiv. Cov tsos mob tseem ceeb yog polyuria thiab polydipsia.

Lactic acidosis tsis nco qab feem ntau tshwm sim hauv cov neeg mob hnub nyoog 50 xyoo thiab tshaj plawv mob raum, mob siab, lossis mob plawv. Nrog rau cov mob no, qhov kev xav ntau ntawm cov kab mob lactic acid tau sau tseg hauv cov ntshav.

Cov phiajcim ua ntej yog hypotension, ua tsis taus pa, tsis tso zis.

Cov teeb meem lig

Tawm tsam keeb kwm ntawm kev mob ntshav qab zib ntev, mob tshwm sim lig uas tsis tuaj yeem kho lossis xav tau kev kho mob ntev dua. Nrog rau ntau hom mob ntawm cov kab mob, lub txim kuj yuav txawv.

Yog li, nrog thawj hom mob ntshav qab zib, mob ntshav qab zib ko taw mob, cataracts, nephropathy, dig muag vim yog retinopathy, mob plawv thiab kab mob hniav feem ntau tsim.Nrog IDDM, mob ntshav qab zib gangrene, retinopathy, retinopathy feem ntau tshwm sim, thiab vascular thiab lub plawv pathologies tsis yog peculiar rau hom mob no.

Nrog cov mob ntshav qab zib retinopathy, cov leeg, hlab ntsha thiab capillaries ntawm retina muaj kev cuam tshuam, vim tias tiv thaiv keeb kwm yav dhau los ntawm tus mob hyperglycemia, cov hlab ntsha nqaim, uas yog vim li cas lawv tsis tau txais ntshav txaus. Raws li qhov tshwm sim, txoj kev hloov pauv tau tshwm sim, thiab qhov tsis muaj pa oxygen pab txhawb qhov tseeb tias lipids thiab calcium ntsev yog debugged hauv qhov retina.

Cov kev hloov pauv pathological ua rau tsim cov nti thiab infiltrates, thiab yog tias muaj qhov exacerbation ntawm ntshav qab zib mellitus, ces tus retina yuav cuam tshuam thiab ib tus neeg yuav ua qhov muag tsis pom, qee zaum muaj mob ntshav qab zib lossis lub ntsej muag txhaws.

Neurological teeb meem kuj tsis yooj yim dua rau cov ntshav qab zib. Neuropathy muaj kev phom sij vim nws ua rau pom qhov ntawm ko taw mob ntshav qab zib, uas yuav ua rau txiav tes taw ntawm tes taw.

Cov ua rau cov hlab ntsha hauv ntshav qab zib tsis tau taub tag nrho. Tab sis ob yam tseem ceeb yog qhov txawv: qhov thib ib yog tias cov piam thaj siab ua rau edema thiab cov hlab ntaws, thiab qhov thib ob uas cov xaim hluav taws xob tsis zoo los ntawm cov khoom noj tsis txaus uas tshwm sim los ntawm vascular puas tsuaj.

Mob ntshav qab zib insulin-mellitus nrog cov leeg mob tuaj yeem ua rau nws tus kheej sib txawv:

  1. Hnov leeg ntshav siab - muaj qhov tsis hnov ​​zoo nyob hauv ob txhais ceg, thiab tom qab ntawd sab caj npab, hauv siab thiab plab.
  2. Urogenital form - tshwm sim thaum txoj hlab ntshav ntawm lub hnab yas pralus tau txais kev puas tsuaj, uas cuam tshuam rau txoj haujlwm ntawm lub zais zis thiab txoj hlab zis.
  3. Mob plawv neuropathy - pom los ntawm kev chuv nqaij.
  4. Lub plab zom mov plab daim ntawv - nws yog tus cwj pwm los ntawm kev ua txhaum ntawm kev hla cov zaub mov los ntawm txoj hlab pas, thaum muaj ib qho ua tsis tiav ntawm kev ua kom lub plab.
  5. Daim tawv nqaij mob neuropathy - ua rau los ntawm kev puas tsuaj rau cov qog ua hws, vim tias daim tawv nqaij ua kom qhuav.

Neurology nyob rau hauv cov ntshav qab zib yog qhov txaus ntshai vim hais tias nyob rau hauv tus txheej txheem ntawm nws txoj kev txhim kho tus neeg mob nres kom hnov ​​mob hypoglycemia. Thiab qhov no tuaj yeem ua rau muaj kev tsis taus lossis tuag taus.

Cov tsos mob ntawm tus mob ntshav tes thiab txhais taw tshwm sim nrog kev puas tsuaj rau cov hlab ntshav thiab cov hlab ntsaws ntawm cov nqaij mos, pob qij txha thiab pob txha. Cov teeb meem no tshwm sim hauv ntau txoj kev, nws tag nrho yog nyob ntawm daim ntawv. Daim ntawv neuropathic tshwm sim hauv 65% ntawm cov xwm txheej ntawm SDS, nrog kev puas tsuaj rau cov hlab ntsha uas tsis xa cov leeg mus rau cov ntaub so ntswg. Nyob rau lub sijhawm no, nruab nrab ntawm cov ntiv tes thiab lub xib taws, cov tawv nqaij ua kom tuab thiab ua paug, thiab tom qab ntawd mob txhab rau nws.

Tsis tas li ntawd, tus ko taw o tuaj thiab nws kub heev. Thiab vim yog kev puas tsuaj rau pob txha nqaj qaum thiab pob txha, txoj kev pheej hmoo ntawm lub cev puas tsuaj nce ntau.

Daim ischemic tsim tawm vim muaj ntshav ntws tsis zoo hauv cov hlab ntsha loj ntawm ko taw. Qhov kev mob puas siab ntsws no ua rau tus ko taw txias dua, ua cyanotic, daj ntseg thiab mob nqaij mob rau nws.

Qhov ntau ntawm cov nephropathy mob ntshav qab zib yog qhov ntau (txog 30%). Qhov kev tsis txaus ntseeg no yog qhov txaus ntshai nyob rau hauv tias yog tias nws tsis tau tshawb pom ua ntej dhau los ntawm kev nce qib, tom qab ntawd nws yuav xaus nrog kev txhim kho ntawm lub raum tsis ua haujlwm.

Hauv hom 1 lossis hom 2 mob ntshav qab zib, lub raum puas yuav sib txawv. Yog li, nrog daim ntawv insulin-tiv thaiv tsis pub tus kab mob, tus kab mob no pib loj tuaj thiab feem ntau thaum tseem hluas.

Thaum nyuam qhuav pib muaj, mob hnyav li ntshav qab zib feem ntau tshwm sim yam tsis muaj qhov tseeb tshwm sim, tab sis qee tus neeg mob yuav tseem muaj cov tsos mob xws li:

  • tsaug zog
  • o tuaj
  • cramps
  • lub plawv tsis ua hauj lwm
  • hnyav
  • dryness thiab khaus ntawm daim tawv nqaij.

Lwm qhov kev qhia ntawm nephropathy yog qhov muaj ntshav nyob hauv cov zis. Txawm li cas los xij, cov tsos mob no tsis tshwm sim ntau.

Thaum tus kab mob mus lawm, ob lub raum tsum tshem tawm cov co toxins los ntawm cov ntshav, thiab lawv pib mus ntxiv rau hauv lub cev, maj mam lom nws. Uremia feem ntau yog nrog ntshav siab thiab tsis meej pem.

Qhov cim qhia txog tus mob nephropathy yog muaj cov protein nyob hauv cov zis, yog li cov neeg mob ntshav qab zib yuav tau kuaj zis tsawg kawg ib xyoos ib zaug. Ua tsis tiav txoj kev kho no yuav ua rau lub raum tsis ua haujlwm, thaum tus neeg mob tsis tuaj yeem nyob tsis muaj ntshav lossis raum hloov raum.

Lub plawv thiab leeg ntshav muaj ntshav qab zib kuj tsis yooj yim dua. Qhov tshwm sim feem ntau ntawm cov pathologies yog atherosclerosis ntawm cov hlab ntshav hlab ntsha uas pub lub plawv. Tus kab mob no tshwm sim thaum cov roj (cholesterol) tso rau ntawm cov hlab ntsha, uas tuaj yeem ua rau lub plawv nres lossis mob stroke.

Tus mob ntshav qab zib kuj tseem nquag lub plawv nres. Nws cov tsos mob ua tsis taus pa, ascites, thiab o ntawm cov ceg.

Tsis tas li ntawd, nyob rau hauv cov neeg muaj ntshav qab zib, qhov kev tsis txaus ntseeg uas tshwm sim feem ntau yog mob ntshav liab.

Nws yog qhov txaus ntshai vim tias nws cuam tshuam ntau qhov kev pheej hmoo ntawm lwm cov teeb meem, suav nrog retinopathy, nephropathy, thiab lub plawv tsis ua haujlwm.

Kev tiv thaiv thiab kho kab mob ntshav qab zib

Cov mob thaum ntxov thiab lig dhau los kho nyob rau ntau txoj kev. Yog li, thiaj li yuav txo tau qhov tshwm sim ntawm cov mob ntshav qab zib uas tshwm sim thaum pib, nws yog ib qho tsim nyog yuav tsum tau soj ntsuam kom tsis tu ncua ntawm qib glycemia, thiab yog tias muaj kev txhim kho hypoglycemic lossis hyperglycemic lub xeev, siv cov kev kho mob tsim nyog hauv lub sijhawm.

Kev kho mob rau kev mob ntshav qab zib hom 1 yog raws li peb yam kev kho mob. Ua ntej tshaj plaws, nws yog qhov tsim nyog los tswj cov theem ntawm cov piam thaj, uas yuav tsum dhau los ntawm 4.4 txog 7 mmol / l. Txog qhov kawg no, lawv siv tshuaj txo cov ntshav qab zib lossis siv tshuaj insulin rau ntshav qab zib.

Nws kuj tseem ceeb kom them nyiaj rau cov txheej txheem metabolic uas cuam tshuam vim yog insulin tsis txaus. Yog li, cov neeg mob tau sau tshuaj alpha-lipoic acid thiab tshuaj vascular. Thiab thaum muaj atherogenicity siab ntau, tus kws kho mob tau sau ntawv rau cov tshuaj uas txo cov roj (fibrates, statins).

Ib qho ntxiv, txhua tus mob tshwj xeeb kho tau. Yog li, nrog thaum ntxov retinopathy, laser photocoagulation ntawm tus retina lossis tshem tawm ntawm lub cev ntawm vitreous (vitrectomy) tau qhia.

Thaum muaj mob nephropathy, siv tshuaj tiv thaiv kev mob ntshav siab, thiab tus neeg mob yuav tsum ua raws li kev noj zaub mov tshwj xeeb. Hauv kev ua rau lub raum tsis ua haujlwm, kev hloov ntshav los yog lub raum ua tau.

Kev kho mob ntshav qab zib muaj teeb meem nrog cov hlab ntaws ua rau cuam tshuam nrog kev noj cov vitamins B. Cov tshuaj no txhim kho cov leeg hauv cov leeg. Cov leeg nqaij so taus xws li carbamazepine, pregabalin lossis gabopentin kuj tau qhia.

Nyob rau hauv cov ntaub ntawv ntawm ntshav qab zib ko taw syndrome, cov haujlwm hauv qab no yog nqa tawm:

  1. dosed lub cev ua si,
  2. tshuaj tua kab mob
  3. hnav khau tshwj xeeb
  4. kho cov qhov txhab.

Kev tiv thaiv ntawm cov teeb meem mob ntshav qab zib mellitus yog kev soj ntsuam kab ke ntawm glycated hemoglobin thiab ntshav hauv cov ntshav.

Nws tseem yog ib qho tseem ceeb los soj ntsuam ntshav siab, uas yuav tsum tsis txhob siab tshaj 130/80 hli Hg.

Tseem, yuav kom tsis txhob mob ntshav qab zib nrog ntau yam mob, nws yog ib qho tsim nyog yuav tau ua cov kev kawm niaj hnub. Cov no suav nrog dopplerography ntawm cov hlab ntsha, tsom xam cov zis, ntshav, kuaj cov nyiaj ntawm lub ntsej muag. Kev sab laj ntawm tus kws kho paj hlwb, kws kho plawv thiab phais leeg nqaij kuj qhia tau.

Txhawm rau ntxuav cov ntshav thiab tiv thaiv teeb meem hauv lub plawv, koj yuav tsum noj Aspirin txhua hnub. Ntxiv rau, cov neeg mob tau qhia kev tawm dag zog lub cev rau cov ntshav qab zib mellitus thiab ua raws li cov zaub mov tshwj xeeb, tsis lees txais cov cwj pwm tsis zoo.

Daim vis dis aus hauv tsab xov xwm no tham txog kev mob ntshav qab zib.

Vim li cas cov kev mob cuam tshuam tshwm sim hauv ntshav qab zib

Qhov ua rau ntawm cov tsos ntawm cov kab mob sib kis yog nyob ntawm seb hom mob. Hauv hom I mob ntshav qab zib mellitus, qhov teeb meem tshwm sim thaum tus neeg mob tsis siv tshuaj insulin kom raws sijhawm.

Tus txheej txheem rau kev txhim kho ntawm cov teeb meem:

  1. Tus nqi ntawm cov insulin hauv cov ntshav txo qis, thiab cov piam thaj nce ntxiv.
  2. Muaj qhov xav zoo ntawm kev nqhis dej, polyuria (nce tso zis ntxiv).
  3. Qhov tshwj xeeb ntawm cov roj ntsha hauv cov ntshav nce vim yog lipolysis loj heev (ua rau cov rog rog).
  4. Tag nrho cov txheej txheem anabolic qeeb dua, cov ntaub so ntswg tsis tuaj yeem paub tseeb tias kev rhuav tshem ntawm ketone lub cev (acetone tsim hauv lub siab).
  5. Muaj kev qaug cawv ntawm lub cev.

Nrog hom II mob ntshav qab zib mellitus (non-insulin-dependant), cov teeb meem tshwm sim vim cov neeg mob tsis xav ua raws li kev noj zaub mov noj thiab tsis noj tshuaj txo ntshav qab zib. Kev kho cov khoom noj khoom haus yog qhov yuav tsum tau ua hauv kev kho mob ntawm tus mob hyperglycemia (ntau dhau ntawm cov piam thaj hauv cov ntshav) thiab cov tshuaj tiv thaiv insulin (txo qis kev cuam tshuam ntawm cov tshuaj insulin-hlwb ua rau kev ua ntawm insulin).

Teeb meem ntawm tus mob ntshav qab zib hom 2 tshwm sim raws li nram no:

  1. Theem cov ntshav qabzib nce zuj zus.
  2. Vim tias muaj suab thaj ntau dhau, kev ua haujlwm ntawm cov nruab nrog sab hauv pib zuj zus.
  3. Intracellular hyperglycemia kev loj hlob, ua rau cov ntshav qabzib neurotoxicity (kev ua haujlwm ntawm cov hlab ntsha tsis zoo) thiab lwm yam kab mob.

Qhov tseeb uas ua rau muaj kev pheej hmoo ntawm cov teeb meem

Tus neeg mob tsis tshua pom kev tsis txaus ntseeg yam tsis muaj laj thawj dabtsi. Qhov tseeb uas ua rau muaj kev pheej hmoo mob ntshav qab zib:

  • Kev tshuaj ntsuam genetic predisposition. Txoj kev pheej hmoo ntawm kev tsim muaj mob hnyav nyob hauv tus neeg mob nce 5-6 zaug yog tias nws ib tus niam txiv muaj kev mob ntshav qab zib.
  • Tshaj qhov hnyav. Qhov no yog qhov txaus ntshai tshaj rau tus mob 2. Kev ua txhaum ntawm kev noj zaub mov tsis zoo ua rau lub cev rog ntxiv. Cov xoos tshwj xeeb hauv xov tooj ntawm tes yuav tsis tuaj yeem cuam tshuam nrog cov tshuaj insulin, thiab ntev mus lawv cov lej hauv cov nqaij tau tsawg dua.
  • Haus cawv. Cov neeg muaj ntshav qab zib txhua yam yuav tsum tso cawv. nws ua rau hypoglycemia, txo cov suab vascular.
  • Tsis ua raws kev noj haus. Nrog ntshav qab zib hom 2, nws yog txwv tsis pub noj cov txiv ntoo qab zib thiab zaub mov uas muaj cov carbohydrates sai thiab cov rog pauv (ice cream, chocolate, margarine, thiab lwm yam). Nrog rau txhua yam kabmob, koj tsis tuaj yeem noj mov sai. Tus mob ntshav qab zib “Insulin” yuav tsum tshem tawm cov khoom qab zib ntawm cov khoom noj. Yog tias kev noj zaub mov tsis ua raws, qib qab zib yuav sawv thiab poob.
  • Tsis muaj kev tawm dag zog. Tsis quav ntsej txog kev tawm dag zog thiab qoj ib ce ua rau lub cev zom cov zaub mov qeeb zuj zus. Cov khoom ua kom lwj yog lub cev ntev dhau thiab lom nws.
  • Tus kab mob plawv mus ntev. Nrog rau kev kub siab, mob plawv, mob ntshav nce siab, mob ntawm cov nqaij mos rau insulin tsawg dua.
  • Kev ntxhov siab, muaj zog ntxhov siab-muaj kev ntxhov siab. Adrenaline, noradrenaline, glucocorticoids cuam tshuam loj heev rau kev ua haujlwm pancreatic thiab insulin ntau lawm.
  • Cev xeeb tub Cov ntaub so ntswg ntawm cov poj niam lub cev nqus tau lawv tus kheej cov insulin tsawg dua vim tias nquag ua cov tshuaj hormones.

Cia Koj Saib